MicroVue™ CIC-Raji Cell Replacement EIA (CIC-C3d)

The MicroVue CIC-Raji Cell Replacement Enzyme Immunoassay measures immune complexes containing C3 activation fragments in human serum and plasma.

Product Specifications


Serum/Plasma 10 μL

Assay Time2.5 hours
Cross Reactivity


Ordering Information

For In Vitro Diagnostic Use.
Catalog NumberA002
Catalog Number (CE) 
Size96 wells/test
Price (USD)$635.00
Price (EURO)565,00 €

Contact us

US Phone+1 (858) 552 1100
EU Phone+353 (91) 412 474
US Emailcontact-us@quidelortho.com
EU Emailcontact-emea@quidelortho.com



The MicroVue CIC-Raji Cell Replacement Enzyme Immunoassay measures immune complexes containing C3 activation fragments in human serum and plasma.

Size96 wells/test

96 well plate with 12 eight-well strips in a resealable foil pouch

SpecimenSerum/Plasma 10 μL
Limit of Detection (LOD)4.0 μg Eq/mL
Lower Limit of Quantitation (LLOQ)N/A
Upper Limit of Quantitation (ULOQ)N/A
Intra Assay3–9%
Inter Assay4–30%
Sample Values

Normal 5.0 μg Eq/mL, SLE 15.8 μg Eq/mL, RA 13.7 μg Eq/mL

Assay Time2.5 hours
Cross Reactivity



Store the unopened kit at 2°C to 8°C. Refer to Product Insert for additional storage details.


The importance of circulating immune complexes (CIC) and their relationship to various diseases has been the subject of investigation for a number of years. Formation of immune complexes is a protective, on-going, and usually benign process of a normally functioning immune system. CIC are removed from the circulation in the normal host by a number of complex biochemical, enzymatic, and cellular processes. The effective clearance of many CIC requires the activation of complement. Complement activation will result in C3 fragment deposition within the immune complex followed by enhanced elimination by phagocytic cells of the reticuloendothelial system. Under certain disease conditions, which are not fully understood, immune complexes may not be efficiently eliminated from the body. In these diseases, the immune complexes may accumulate and initiate complement-dependent injury in various organs and tissues. This activation of complement may begin a series of potentially destructive events in the host including anaphylatoxin production, cell lysis, leukocyte stimulation, and activation of macrophages and other cells. When immune complexes become fixed to vessel walls or cell membranes, destruction of normal tissue can occur, as in some cases of glomerulonephritis. Certain properties of CIC influence their potential pathogenicity. Of particular importance are: (1) nature, size and concentration of the antigen; (2) nature, size and concentration of the antibody; (3) rate of formation and clearance of the immune complexes. Circulating immune complexes have been measured in a variety of conditions: for example, infections, autoimmune disorders, trauma, and neoplastic proliferative diseases. Current studies suggest that CIC determinations can be important in the evaluation of certain diseases and, sometimes, in monitoring efficiency of therapy. This is especially true in systemic lupus erythematosus (SLE) and some forms of rheumatoid arthritis (RA). The first disease state linked to the formation of immune complexes was serum sickness, described in the early 1900’s by von Pirquet. Since that time elevated levels of CIC have been described in autoimmune diseases (SLE, SLE-related syndrome, RA), glomerulonephritis, neoplastic disease (Hodgkin’s, leukemia), bacterial infections (subacute bacterial endocarditis, leprosy), parasitic infections (malaria, schistosomiasis) and viral infections (hepatitis, mononucleosis). Over 40 assay techniques to detect or quantitate CIC have been described. Such tests as the Raji Cell assay, C1q deviation test, conglutinin test, fluid phase C1q binding procedures, rheumatoid factor assay, PEG precipitin test, and solid phase C1q assays have been described. Since the size and physiochemical properties of CIC vary markedly, none of these assays has been accepted as a standard. A collaborative study sponsored by the World Health Organization in 1978 determined that no single method was appropriate in all suspected disease states and recommended that at least two different assay techniques be performed to detect and measure CIC adequately.